Gastric atrophy and intestinal metaplasia changes 8 years after Helicobacter pylori eradication. A blind, randomised study

Abstract

Background: Chronic atrophic gastritis and intestinal metaplasia are regarded as predisposing factors for gastric cancer associated with Helicobacter pylori infection, and their severity appears to influence gastric cancer risk. Our purpose was to determine the outcome of chronic gastritis after H. pylori eradication in a long-term follow-up.

Methods: Fifty-four consecutive patients with duodenal ulcer and H. pylori infection were enrolled in the study. Endoscopic examination with antral and corporal biopsy was done at baseline and yearly after conventional eradication therapy (omeprazole 40 mg b.i.d., amoxocyllin 1 g b.i.d and clarithromycin 500 mg b.i.d.). Gastritis, atrophy, and metaplasia were graded according to the updated Sydney System.

Results: Twenty-four patients were successfully treated; infection persisted in 14 and 16 dropped out (during the first 5 years of follow-up). Inflammation and mean neutrophil activity significantly decreased in patients in whom H. pylori was eradicated. Glandular atrophy improved in 2 and disappeared in 5/17 patients, whereas intestinal metaplasia improved in 3 and disappeared in 2/12. In the patients in whom H. pylori persisted, inflammatory infiltrate, atrophy and intestinal metaplasia had not significantly decreased during follow-up. In contrast, glandular atrophy worsened in 2 and developed in 5/7 patients. Similarly, intestinal metaplasia did not improve when present and developed in 5/13 cases.

Conclusions: In a long-term follow-up, H. pylori eradication does not affect glandular atrophy, but it seems to prevent the development of precancerous lesions such as intestinal metaplasia.